Live Cell Labeling of Glial Progenitor Cells Using Targeted Quantum Dots

This study describes the development of targeted quantum dots (T-QDs) as biomarkers for the labeling of glial progenitor cells (GPCs) that over express platelet derived growth factor (PDGF) and its receptor PDGFR (GPC^PDGF). PDGFR plays a critical role in glioma development and growth, and is also known to affect multiple biological processes such as cell migration and embryonic development. T-QDs were developed using streptavidin-conjugated quantum dots (S-QDs) with biotinylated antibodies and utilized to label the intracellular and extracellular domains of live, cultured GPC^PDGF cells via lipofection with cationic liposomes. Confocal studies illustrate successful intracellular and extracellular targeted labeling within live cells that does not appear to impact upstream PDGFR dynamics during real-time signaling events. Further, T-QDs were nontoxic to GPC^PDGF cells, and did not alter cell viability or proliferation over the course of 6 days. These results raise new applications for T-QDs as ultra sensitive agents for imaging and tracking of protein populations within live cells, which that will enable future mechanistic study of oncogenic signaling events in real-time.     

Stimulation-induced parkinsonism after posteroventral deep brain stimulation of the globus pallidus internus for craniocervical dystonia

The authors report on a patient with craniocervical dystonia who was treated with bilateral GPi stimulation, with excellent improvement in dystonia but at the cost of stimulation-induced, reversible parkinsonism. Stimulation through ventral contacts resulted in maximal relief of craniocervical dystonia but induced considerable hypophonia, bradykinesia, rigidity, freezing, and impaired postural reflexes. Stimulation through dorsal contacts alleviated parkinsonism, but resulted in the return of dystonia. No stimulation parameters could alleviate the dystonia without inducing parkinsonism over the course of his 4-year follow-up.     

Management of hepatitis B virus

Hepatitis B is a common problem worldwide with serious sequelae. Despite the explosion of new agents, management has grown even more complicated. The treatment paradigm is evolving from limited therapy to lifelong viral suppression in several populations. This shift has been a direct result of not only well-tolerated oral medications, but also the increasing recognition that active viral replication leads to untoward events such as cirrhosis, liver failure and hepatocellular carcinoma. However, therapy is not without risk, which includes side effects, cost and drug resistance. Controversy surrounds several clinical questions, including which patients are eligible for therapy, which treatment is optimal and at what point may therapy be discontinued. This commentary will discuss these questions as well as the limitations of the literature used to support our current treatment recommendations.     

Autologous Serum Therapy in Chronic Urticaria

Autologous serum therapy is a promising therapy for treatment resistant urticaria. This is useful in developing countries as this is economical option. Minimum instruments like centrifuge, syringe and needles are required for the procedure.     

The effects of nicotine on the alpha-7 and beta-2 nicotinic acetycholine receptor subunits in the developing piglet brainstem

Exposure to cigarette smoke is a major risk factor for sudden infant death syndrome (SIDS). We tested the hypothesis that nicotine increases expression of the nicotinic acetylcholine receptor (nAChR) subunits α7 and β2 in a piglet model. Piglets exposed to 2 mg/kg/day nicotine for 14 days postnatally (n = 14) were compared to non-exposed controls (n = 14), (equal gender proportions). Immunohistochemistry was performed to identify and quantify changes in, α7 and β2 nAChR subunits in 8 nuclei of the medulla at both the rostral and caudal levels. Compared to controls, nicotine exposed piglets had decreased α7 in the rostral dorsal motor nucleus of the vagus (rDMNV) (p = 0.01), and increased β2 in the caudal DMNV (cDMNV) (p = 0.05), caudal nucleus of the spinal trigeminal tract (cNSTT) (p = 0.03) and caudal nucleus of the solitary tract (cNTS) (p = 0.04). Analysis by gender showed that in the control group, compared to males, females had higher β2 in the caudal hypoglossal (cXII) (p < 0.01) and caudal inferior olivary (p = 0.04) nuclei, while in the nicotine group females had higher β2 in the cDMNV (p = 0.02). Compared to control males, nicotine exposed males had lower β2 in the cXII (p < 0.01). Overall, changes in α7 were specific to nicotine exposure with no gender differentiation. Changes in β2 were more widespread but showed gender-specific effects. These findings provide evidence that early postnatal exposure to nicotine significantly affects nAChR subunit expressions in the developing brainstem.